However, as the parasite penetrated the host cell, MIC2 was excluded from entering the vacuole, while ROP1 ®lled the parasitophorous vacuole (Fig. 5, second row). MIC2 was progressively capped behind the moving junction and remained con®ned to the portion of the parasite that still protruded from the host cell (Fig. 5, third row). The absence of MIC2 on the apical surface of partially internalized parasites implies that secretion may be terminated rapidly upon entry. At the completion of invasion, MIC2 was not detected within the vacuole or on the host cell surface, suggesting that it was released into the surrounding medium (Fig. 5, bottom row). Cryo-immunoelectron microscopy con®rmed that MIC2 was localized to the interface that forms between host and parasite membranes during invasion (Fig. 6). This interface was not limited to the moving junction, but extended along the lateral aspects
However, as the parasite penetrated the host cell, MIC2 was excluded from entering the vacuole, while ROP1 ®lled the parasitophorous vacuole (Fig. 5, second row). MIC2 was progressively capped behind the moving junction and remained con®ned to the portion of the parasite that still protruded from the host cell (Fig. 5, third row). The absence of MIC2 on the apical surface of partially internalized parasites implies that secretion may be terminated rapidly upon entry. At the completion of invasion, MIC2 was not detected within the vacuole or on the host cell surface, suggesting that it was released into the surrounding medium (Fig. 5, bottom row). Cryo-immunoelectron microscopy con®rmed that MIC2 was localized to the interface that forms between host and parasite membranes during invasion (Fig. 6). This interface was not limited to the moving junction, but extended along the lateral aspects
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